Fike J R, Cann C E, Turowski K, Higgins R J, Chan A S, Phillips T L, Davis R L
Department of Radiation Oncology, School of Medicine, University of California, San Francisco 94143.
Int J Radiat Oncol Biol Phys. 1988 Jan;14(1):63-70. doi: 10.1016/0360-3016(88)90052-1.
Dose response relationships were determined after hemibrain x-irradiation of normal beagle dogs. Radiation doses of 11.5, 13.5, 14.3, and 17 Gy were delivered in a single dose and results were compared to previous studies using doses of 15 and 30 Gy. Brain injury was quantified using computed tomography (CT), with serial studies obtained monthly up to 1 year following irradiation. Quantitative endpoints included low density volume and contrast enhancement. Doses above 14.3 Gy resulted in high lethality 5-8 months following irradiation, and an LD50 of 14.9 Gy was calculated. At these lethal doses, low density volume representing edema, demyelination, and necrosis had a similar response with an ED50 of 14.6 Gy. Radiation-induced decreases in white matter density appeared 5-6 months after sublethal doses (less than or equal to 14.3 Gy) and the volume of tissue characterized by this low density increased with time and dose. This sublethal low density change had an ED50 of 12.8 Gy, and may reflect a loss or generalized atrophy of glial cells and/or myelin. These results show that: (a) the dose response curves obtained after hemibrain x-irradiation are extremely steep; and (b) at least two processes may be involved in the development of late radiation damage, one that is rapid upon onset (a "delayed acute" reaction) and the other which is a slower and more degenerative process.
对正常比格犬进行半脑X线照射后确定剂量反应关系。单次给予11.5、13.5、14.3和17 Gy的辐射剂量,并将结果与先前使用15和30 Gy剂量的研究进行比较。使用计算机断层扫描(CT)对脑损伤进行量化,在照射后长达1年的时间里每月进行系列研究。定量终点包括低密度体积和对比增强。14.3 Gy以上的剂量在照射后5 - 8个月导致高致死率,并计算出LD50为14.9 Gy。在这些致死剂量下,代表水肿、脱髓鞘和坏死的低密度体积有相似的反应,ED50为14.6 Gy。亚致死剂量(小于或等于14.3 Gy)后5 - 6个月出现辐射诱导的白质密度降低,以这种低密度为特征的组织体积随时间和剂量增加。这种亚致死性低密度变化的ED50为12.8 Gy,可能反映了神经胶质细胞和/或髓鞘的丢失或普遍萎缩。这些结果表明:(a)半脑X线照射后获得的剂量反应曲线极其陡峭;(b)晚期辐射损伤的发展可能涉及至少两个过程,一个是发病迅速(“延迟急性”反应),另一个是较慢且更具退行性的过程。